Spinal beta-endorphin analgesia involves an interaction with local monoaminergic systems.
Male; Animals; Rats; Adrenergic alpha-Antagonists/pharmacology; Injections; Serotonin Antagonists/pharmacology; Naltrexone/pharmacology; Spinal Cord/*drug effects; Biogenic Monoamines/*physiology; Analgesics/administration & dosage/antagonists & inhibitors/*pharmacology; beta-Endorphin/administration & dosage/antagonists & inhibitors/*pharmacology; Norepinephrine/physiology; Serotonin/physiology; Inbred Strains; Spinal
beta-Endorphin administered intrathecally (i.t.) in rats produced a dose-dependent elevation in tail-flick latency. Naltrexone administered i.t. as a pretreatment reversed the spinal antinociceptive action of beta-endorphin, suggesting that the opioid interacts directly with spinal opiate receptors. Spinal administration of the alpha 1-adrenoceptor antagonist WB-4101 failed to alter the analgesic effects of the opioid, whereas the alpha 2-adrenoceptor antagonist yohimbine completely blocked beta-endorphin-induced elevations in tail-flick latency. Thus, there is an apparent specificity for the alpha
Crisp T; Stafinsky J L; Hess J E; Uram M
European journal of pharmacology
1989
1989-01
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
The antinociceptive effects of 3,4-methylenedioxymethamphetamine (MDMA) in the rat.
Male; Animals; Rats; Analgesics/*pharmacology; Methysergide/pharmacology; Naltrexone/pharmacology; Amphetamines/*pharmacology; Pain/*metabolism; Morphine/pharmacology; Dose-Response Relationship; Drug; Inbred Strains; Receptors; 3; N-Methyl-3; 4-methylenedioxyamphetamine; 4-Methylenedioxyamphetamine/analogs & derivatives/*pharmacology; Serotonin/drug effects/*physiology
The antinociceptive effects of MDMA and morphine were examined in rats using the tail-flick and hot-plate analgesiometric tests. MDMA, in the dose range of 1.5-6.0 mg/kg IP, produced a dose-dependent elevation in hot-plate latency, but did not elevate tail-flick latency. In contrast, morphine (2-8 mg/kg, IP) produced analgesia on both the tail-flick and hot-plate tests in a dose-dependent manner. Neither the opiate antagonist naltrexone nor the adrenoceptor antagonist phentolamine effectively attenuated MDMA-induced analgesia. Conversely, the serotonin antagonist methysergide significantly reversed the analgesic effects of MDMA on the hot-plate test. These findings suggest that the antinociceptive effects of MDMA are serotonergically mediated. Furthermore, the results verify earlier findings describing the test-specific effects of serotonin-induced pain modulation.
Crisp T; Stafinsky J L; Boja J W; Schechter M D
Pharmacology, biochemistry, and behavior
1989
1989-11
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0091-3057(89)90547-9" target="_blank" rel="noreferrer noopener">10.1016/0091-3057(89)90547-9</a>
The noradrenergic component contributing to spinal fentanyl-induced antinociception is supraspinally mediated.
Adrenergic Antagonists; Analgesics/*pharmacology; Animals; Fentanyl/*pharmacology; Injections; Intraventricular; Male; Methysergide/pharmacology; Naltrexone/pharmacology; Norepinephrine/*physiology; Pain Measurement/drug effects; Phentolamine/pharmacology; Rats; Reaction Time/drug effects; Serotonin Antagonists; Spinal; Spinal Cord/*physiology; Sprague-Dawley
1. Male Sprague-Dawley rats were fitted with intrathecal (i.t.) and intracerebroventricular (i.c.v.) catheters. Fentanyl was injected either i.t. or i.c.v., and the antinociceptive efficacy of fentanyl was evaluated using the tail-flick analgesiometric assay. 2. Fentanyl dose-dependently elevated tail-flick latency (TFL) following i.c.v. or i.t. administration. The antinociceptive effects of fentanyl were reversed by naltrexone. 3. Experiments were also designed to evaluate the effects of serotonin and alpha-adrenoceptor antagonists on i.t. or i.c.v. fentanyl-induced elevations in TFL. 4. Phentolamine administered i.t. reversed both the spinal and supraspinal antinociceptive effects of fentanyl, whereas i.t. methysergide did not significantly alter the i.t. or i.c.v. effects of the mu agonist. 5. These data suggest that fentanyl-induced antinociception does not rely on local serotonergic neuronal activation. Due to the highly lipophilic nature of fentanyl, it is possible that the noradrenergic component contributing to spinal fentanyl-induced analgesia is supraspinally-mediated.
Crisp T; Stafinsky J L; Perni V C; Uram M
General pharmacology
1992
1992-11
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0306-3623(92)90291-q" target="_blank" rel="noreferrer noopener">10.1016/0306-3623(92)90291-q</a>
Serotonin contributes to the spinal antinociceptive effects of morphine.
Adrenergic alpha-Antagonists/pharmacology; Adrenergic Antagonists; Analgesics/*pharmacology; Animals; Biogenic Monoamines/physiology; Dose-Response Relationship; Drug; Inbred Strains; Injections; Male; Morphine/*pharmacology; Naltrexone/pharmacology; Nerve Endings/drug effects; Opioid/drug effects; Rats; Reaction Time; Receptors; Serotonin Antagonists/pharmacology; Serotonin/*physiology; Spinal; Spinal Cord/*drug effects
This study was designed to determine if morphine administered intrathecally (IT) interacts with serotonergic or noradrenergic nerve terminals in the spinal cord to produce analgesia on the spinally mediated tail-flick test. Male Sprague-Dawley rats were fitted with IT catheters. One week later, animals were spinally pretreated with receptor antagonists selective for opioid, serotonin or alpha-adrenoceptors, and the ability of these agents to alter spinal morphine-induced antinociception was assessed. Morphine dose-dependently elevated tail-flick latency in a naltrexone-reversible manner. The serotonin receptor antagonists spiroxatrine (5-HT1A), pindolol (5-HT1B), ritanserin (5-HT2) and ICS
Crisp T; Stafinsky J L; Uram M; Perni V C; Weaver M F; Spanos L J
Pharmacology, biochemistry, and behavior
1991
1991-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0091-3057(91)90133-m" target="_blank" rel="noreferrer noopener">10.1016/0091-3057(91)90133-m</a>